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    Evaluative means for detecting inflammatory reactivity
    1.
    发明授权
    Evaluative means for detecting inflammatory reactivity 失效
    用于检测炎症反应性的评估手段

    公开(公告)号：US5006330A

    公开(公告)日：1991-04-09

    申请号：US277708

    申请日：1988-11-30

    Applicant: Esther M. Sternberg ,  Ronald L. Wilder ,  George P. Chrousos ,  Philip W. Gold

    Inventor： Esther M. Sternberg ,  Ronald L. Wilder ,  George P. Chrousos ,  Philip W. Gold

    IPC: G01N33/74 ,  A61K31/40 ,  A61K31/495 ,  G01N33/50

    CPC classification number: G01N33/5091 ,  A61K31/40 ,  A61K31/495 ,  Y10S514/825

    Abstract: Inbred Lewis (LEW/N) female rats develop an arthritis in response to Group A streptococcal cell wall peptidoglycanpolysaccharide (SCW) which mimics human rheumatoid arthritis. Histocompatible Fischer (F344/N) rats, on the other hand, do not develop arthritis in response to the same SCW stimulus. To evaluate this difference in inflammatory reactivity between the two strains, the function of the hypothalamic-pituitary-adrenal axis and its ability to modulate the development of the inflammatory response was studied. It has been found that, in contrast to F344/N rats, LEW/N rats had markedly impaired plasma ACTH and corticosterone responses to SCW, recombinant human Interleukin-1 alpha (IL-1 alpha), the serotonin agonist, quipazine, and synthetic rat corticotropin-releasing hormone (CRH). In addition, LEW/N rats compared to F344/N rats had smaller adrenal glands and larger thymuses. Treatment of LEW/N rats with replacement doses of dexamethasone decreased the severity of their SCW-induced arthritis. Conversely, treatment of F344/N rats with the glucocorticoid receptor antagonist, RU 486, or the serotonin (5-HT.sub.2) antagonist, LY53857, was associated with development of severe inflammatory disease, including arthritis, in response to SCW. These findings support the concept that susceptibility of LEW/N rats to SCW arthritis is related to abnormal hypothalamic-pituitary-adrenal (HPA) axis responsiveness to inflammatory and other stress mediators and that resistance of F344/N rats to SCW arthritis is regulated by an intact HPA axis-immune system feedback loop.

    Abstract translation: 近交路易斯（LEW / N）雌性大鼠针对模拟人类类风湿关节炎的A组链球菌细胞壁肽聚糖多糖（SCW）产生关节炎。 另一方面，组织相容性Fischer（F344 / N）大鼠不会对相同的SCW刺激产生关节炎。 为了评估两种菌株之间的炎症反应性差异，研究了下丘脑 - 垂体 - 肾上腺轴的功能及其调节炎症反应发展的能力。 已经发现，与F344 / N大鼠相比，LEW / N大鼠对SCW，重组人白细胞介素-1α（IL-1α），血清素激动剂，喹地平和合成的血浆ACTH和皮质酮反应明显受损 大鼠促肾上腺皮质激素释放激素（CRH）。 此外，与F344 / N大鼠相比，LEW / N大鼠具有较小的肾上腺和较大的胸腺。 用替代剂量的地塞米松治疗LEW / N大鼠降低其SCW诱导的关节炎的严重程度。 相反，用糖皮质激素受体拮抗剂RU 486或5-羟色胺（5-HT2）拮抗剂LY53857处理F344 / N大鼠与SCW相关的严重炎症性疾病（包括关节炎）的发展有关。 这些发现支持LEW / N大鼠对SCW关节炎的易感性与异常的下丘脑 - 垂体 - 肾上腺（HPA）轴对炎症和其他应激介质的反应性有关的概念，F344 / N大鼠对SCW关节炎的抵抗力由 完整的HPA轴免疫系统反馈回路。

    Evaluative means for detecting inflammatory reactivity
    3.
    发明授权
    Evaluative means for detecting inflammatory reactivity 失效
    用于检测炎症反应性的评估手段

    公开(公告)号：US5209920A

    公开(公告)日：1993-05-11

    申请号：US412294

    申请日：1989-09-25

    Applicant: Esther M. Sternberg ,  Ronald L. Wilder ,  Philip W. Gold ,  George P. Chrousos

    Inventor： Esther M. Sternberg ,  Ronald L. Wilder ,  Philip W. Gold ,  George P. Chrousos

    IPC: A61K31/135 ,  A61K31/35 ,  A61K31/365 ,  A61K31/40 ,  A61K31/485 ,  A61K31/495 ,  A61K31/565 ,  A61K31/57 ,  A61K31/585 ,  A61K38/22 ,  A61K45/06 ,  G01N33/50 ,  G01N33/564 ,  G01N33/74

    CPC classification number: A61K31/135 ,  A61K31/35 ,  A61K31/365 ,  A61K31/40 ,  A61K31/485 ,  A61K31/495 ,  A61K31/565 ,  A61K31/57 ,  A61K31/585 ,  A61K38/11 ,  A61K38/2228 ,  A61K45/06 ,  G01N33/5091 ,  G01N33/564 ,  G01N33/74 ,  G01N33/743 ,  G01N2800/102 ,  Y10S435/975 ,  Y10S514/805 ,  Y10S514/825 ,  Y10S514/885 ,  Y10S514/886 ,  Y10S514/889

    Abstract: Inbred Lewis (LEW/N) female rats develop an arthritis in response to Group A streptococcal cell wall peptidoglycanpolysaccharide (SCW) which mimics human rheumatoid arthritis. Histocompatible Fischer (F344/N) rats, on the other hand, do not develop arthritis in response to the same SCW stimulus. To evaluate this difference in inflammatory reactivity between the two strains, the function of the hypothalamic-pituitary-adrenal axis and its ability to modulate the development of the inflammatory response was studied. It has been found that, in contrast to F344/N rats, LEW/N rats had markedly impaired plasma ACTH and corticosterone responses to SCW, recombinant human Interleukin-1 alpha (IL-1 alpha), the serotonin agonist, quipazine, and synthetic rat corticotropin-releasing hormone (CRH). In addition, LEW/N rats compared to F344/N rats had smaller adrenal glands and larger thymuses. Treatment of LEW/N rats with replacement doses of dexamethasone decreased the severity of their SCW-induced arthritis. Conversely, treatment of F344/N rats with the glucocorticoid receptor antagonist, RU 486, or the serotonin (5-HT.sub.2) antagonist, LY53857, was associated with development of severe inflammatory disease, including arthritis, in response to SCW. These findings support the concept that susceptibility of LEW/N rats to SCW arthritis is related to abnormal hypothalamic-pituitary-adrenal (HPA) axis responsiveness to inflammatory and other stress mediators and that resistance of F344/N rats to SCW arthritis is regulated by an intact HPA axis-immune system feedback loop.

    Abstract translation: 近交路易斯（LEW / N）雌性大鼠针对模拟人类类风湿关节炎的A组链球菌细胞壁肽聚糖多糖（SCW）产生关节炎。 另一方面，组织相容性Fischer（F344 / N）大鼠不会对相同的SCW刺激产生关节炎。 为了评估两种菌株之间的炎症反应性差异，研究了下丘脑 - 垂体 - 肾上腺轴的功能及其调节炎症反应发展的能力。 已经发现，与F344 / N大鼠相比，LEW / N大鼠对SCW，重组人白细胞介素-1α（IL-1α），血清素激动剂，喹地平和合成的血浆ACTH和皮质酮反应明显受损 大鼠促肾上腺皮质激素释放激素（CRH）。 此外，与F344 / N大鼠相比，LEW / N大鼠具有较小的肾上腺和较大的胸腺。 用替代剂量的地塞米松治疗LEW / N大鼠降低其SCW诱导的关节炎的严重程度。 相反，用糖皮质激素受体拮抗剂RU 486或5-羟色胺（5-HT2）拮抗剂LY53857处理F344 / N大鼠与SCW相关的严重炎症性疾病（包括关节炎）的发展有关。 这些发现支持LEW / N大鼠对SCW关节炎的易感性与异常的下丘脑 - 垂体 - 肾上腺（HPA）轴对炎症和其他应激介质的反应性有关的概念，F344 / N大鼠对SCW关节炎的抵抗力由 完整的HPA轴免疫系统反馈回路。

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